1
NURS 5315 Advanced Pathophysiology Test Bank
2025–2026 | 180 NCLEX-Style Questions & Detailed
Rationales | McCance & Huether UTA A+ Resource
1.
A 64-year-old male presents to the clinic with progressive shortness of breath over
the past 6 months, difficulty lying flat at night, and swelling in both ankles. Vital
signs reveal blood pressure of 158/92 mm Hg, heart rate 96 bpm, and oxygen
saturation 92% on room air. Cardiac auscultation reveals an S3 gallop, and lung
auscultation detects bibasilar crackles. Which underlying pathophysiologic change
is most directly responsible for this patient’s symptoms?
A. Decreased preload
B. Increased left ventricular end-diastolic pressure
C. Reduced systemic vascular resistance
D. Increased coronary artery perfusion
Correct Answer: B. Increased left ventricular end-diastolic pressure
Rationale:
In chronic left-sided heart failure, as seen in this patient, decreased contractility
and increased afterload from hypertension result in elevated left ventricular end-
diastolic pressure. This increased pressure is transmitted backward into the
pulmonary veins, causing pulmonary congestion (manifesting as dyspnea and
orthopnea) and the development of an S3 gallop due to rapid ventricular filling
during early diastole. The same elevated venous pressures eventually cause fluid
accumulation in the systemic circulation, leading to ankle edema. Option A is
incorrect because preload is typically elevated, not reduced, in systolic heart
, 2
failure. Option C is incorrect because systemic vascular resistance is usually
increased in response to neurohormonal activation (RAAS and sympathetic
nervous system) in heart failure. Option D is incorrect because coronary perfusion
is often impaired, not increased, in heart failure due to reduced diastolic filling
time and elevated ventricular pressures (McCance & Huether, pp. 1184–1185).
2.
A 42-year-old female presents with sharp, stabbing chest pain that worsens with
deep inspiration and improves when she sits up and leans forward. She reports a
recent upper respiratory infection one week ago. Physical examination reveals a
pericardial friction rub best heard along the left lower sternal border with the
patient leaning forward. An ECG shows diffuse ST-segment elevations and PR
depressions. Which finding is most characteristic of her condition?
A. Widened pulse pressure
B. Pericardial friction rub
C. Jugular venous distention without hypotension
D. Bounding peripheral pulses
Correct Answer: B. Pericardial friction rub
Rationale:
Acute pericarditis, often post-viral, presents with pleuritic chest pain that improves
with sitting forward, a pericardial friction rub due to inflamed pericardial layers
rubbing together, and ECG findings of diffuse ST elevation and PR depression.
The friction rub is the most characteristic finding and can be heard in nearly all
cases at some point during the illness. Option A, widened pulse pressure, is more
consistent with aortic regurgitation and not pericarditis. Option C, jugular venous
distention without hypotension, is more typical of right-sided heart failure or
isolated pulmonary hypertension. Option D, bounding peripheral pulses, are
associated with hyperdynamic circulation such as in aortic regurgitation or
thyrotoxicosis, not acute pericarditis (McCance & Huether, p. 1208).
3.
A 58-year-old male with a 15-year history of poorly controlled hypertension
, 3
undergoes an echocardiogram that reveals increased left ventricular wall thickness
with a small chamber size. He denies chest pain but reports mild exertional
dyspnea. Which mechanism best explains his cardiac remodeling?
A. Increased preload leading to elongation of myocardial cells
B. Increased afterload causing parallel replication of sarcomeres
C. Myocardial infarction leading to collagen deposition
D. Sympathetic activation increasing myocardial contractility
Correct Answer: B. Increased afterload causing parallel replication of sarcomeres
Rationale:
In chronic hypertension, the sustained increase in afterload forces the left ventricle
to generate higher pressures to eject blood, resulting in concentric hypertrophy.
This type of hypertrophy occurs due to parallel replication of sarcomeres, which
thickens the ventricular wall without increasing chamber size. Option A describes
eccentric hypertrophy, where sarcomeres are added in series, typically in response
to volume overload conditions such as valvular regurgitation. Option C refers to
post-myocardial infarction remodeling with scar formation, which does not match
this patient’s preserved systolic function. Option D, increased sympathetic
activation, can acutely increase contractility but does not account for structural
hypertrophy seen on echocardiography (McCance & Huether, pp. 1125–1126).
4.
A 70-year-old female presents with chest pressure and diaphoresis. ECG reveals
ST-segment elevations in leads II, III, and aVF. Serial cardiac biomarkers are
drawn. Which marker is most specific for myocardial necrosis in this patient?
A. CK-MB
B. Myoglobin
C. Troponin I
D. LDH-1
Correct Answer: C. Troponin I
Rationale:
Troponin I is the most specific and sensitive biomarker for myocardial necrosis. It
, 4
begins to rise within 3–4 hours after myocardial injury, peaks at 10–24 hours, and
remains elevated for 7–10 days, making it ideal for diagnosing both acute and
recent infarctions. CK-MB is relatively specific for cardiac muscle but returns to
baseline within 48–72 hours, making it less useful for late diagnosis. Myoglobin
rises quickly but is nonspecific, as it is present in all muscle tissue. LDH-1 is
outdated as a diagnostic marker due to poor specificity and delayed elevation
(McCance & Huether, p. 1202).
5.
A 76-year-old male with a long history of a heart murmur reports progressive
exertional dyspnea, chest pain, and episodes of dizziness. Physical examination
reveals a late-peaking systolic murmur at the right second intercostal space
radiating to the carotids and diminished carotid upstrokes. Which pathophysiologic
change is occurring in his left ventricle?
A. Eccentric hypertrophy from volume overload
B. Concentric hypertrophy from pressure overload
C. Myocyte atrophy from reduced workload
D. Chamber dilation from reduced compliance
Correct Answer: B. Concentric hypertrophy from pressure overload
Rationale:
Aortic stenosis creates a fixed outflow obstruction that increases left ventricular
afterload. In response, the myocardium undergoes concentric hypertrophy,
characterized by parallel addition of sarcomeres that thicken the ventricular wall
while preserving chamber size. This adaptation helps maintain cardiac output but
eventually reduces ventricular compliance and contributes to diastolic dysfunction.
Option A, eccentric hypertrophy, occurs with chronic volume overload (e.g., mitral
or aortic regurgitation). Option C, myocyte atrophy, is not a feature of aortic
stenosis. Option D, chamber dilation, can occur in the later stages of aortic stenosis
when systolic dysfunction develops, but early disease is defined by hypertrophy
without dilation (McCance & Huether, pp. 1189–1190).
NURS 5315 Advanced Pathophysiology Test Bank
2025–2026 | 180 NCLEX-Style Questions & Detailed
Rationales | McCance & Huether UTA A+ Resource
1.
A 64-year-old male presents to the clinic with progressive shortness of breath over
the past 6 months, difficulty lying flat at night, and swelling in both ankles. Vital
signs reveal blood pressure of 158/92 mm Hg, heart rate 96 bpm, and oxygen
saturation 92% on room air. Cardiac auscultation reveals an S3 gallop, and lung
auscultation detects bibasilar crackles. Which underlying pathophysiologic change
is most directly responsible for this patient’s symptoms?
A. Decreased preload
B. Increased left ventricular end-diastolic pressure
C. Reduced systemic vascular resistance
D. Increased coronary artery perfusion
Correct Answer: B. Increased left ventricular end-diastolic pressure
Rationale:
In chronic left-sided heart failure, as seen in this patient, decreased contractility
and increased afterload from hypertension result in elevated left ventricular end-
diastolic pressure. This increased pressure is transmitted backward into the
pulmonary veins, causing pulmonary congestion (manifesting as dyspnea and
orthopnea) and the development of an S3 gallop due to rapid ventricular filling
during early diastole. The same elevated venous pressures eventually cause fluid
accumulation in the systemic circulation, leading to ankle edema. Option A is
incorrect because preload is typically elevated, not reduced, in systolic heart
, 2
failure. Option C is incorrect because systemic vascular resistance is usually
increased in response to neurohormonal activation (RAAS and sympathetic
nervous system) in heart failure. Option D is incorrect because coronary perfusion
is often impaired, not increased, in heart failure due to reduced diastolic filling
time and elevated ventricular pressures (McCance & Huether, pp. 1184–1185).
2.
A 42-year-old female presents with sharp, stabbing chest pain that worsens with
deep inspiration and improves when she sits up and leans forward. She reports a
recent upper respiratory infection one week ago. Physical examination reveals a
pericardial friction rub best heard along the left lower sternal border with the
patient leaning forward. An ECG shows diffuse ST-segment elevations and PR
depressions. Which finding is most characteristic of her condition?
A. Widened pulse pressure
B. Pericardial friction rub
C. Jugular venous distention without hypotension
D. Bounding peripheral pulses
Correct Answer: B. Pericardial friction rub
Rationale:
Acute pericarditis, often post-viral, presents with pleuritic chest pain that improves
with sitting forward, a pericardial friction rub due to inflamed pericardial layers
rubbing together, and ECG findings of diffuse ST elevation and PR depression.
The friction rub is the most characteristic finding and can be heard in nearly all
cases at some point during the illness. Option A, widened pulse pressure, is more
consistent with aortic regurgitation and not pericarditis. Option C, jugular venous
distention without hypotension, is more typical of right-sided heart failure or
isolated pulmonary hypertension. Option D, bounding peripheral pulses, are
associated with hyperdynamic circulation such as in aortic regurgitation or
thyrotoxicosis, not acute pericarditis (McCance & Huether, p. 1208).
3.
A 58-year-old male with a 15-year history of poorly controlled hypertension
, 3
undergoes an echocardiogram that reveals increased left ventricular wall thickness
with a small chamber size. He denies chest pain but reports mild exertional
dyspnea. Which mechanism best explains his cardiac remodeling?
A. Increased preload leading to elongation of myocardial cells
B. Increased afterload causing parallel replication of sarcomeres
C. Myocardial infarction leading to collagen deposition
D. Sympathetic activation increasing myocardial contractility
Correct Answer: B. Increased afterload causing parallel replication of sarcomeres
Rationale:
In chronic hypertension, the sustained increase in afterload forces the left ventricle
to generate higher pressures to eject blood, resulting in concentric hypertrophy.
This type of hypertrophy occurs due to parallel replication of sarcomeres, which
thickens the ventricular wall without increasing chamber size. Option A describes
eccentric hypertrophy, where sarcomeres are added in series, typically in response
to volume overload conditions such as valvular regurgitation. Option C refers to
post-myocardial infarction remodeling with scar formation, which does not match
this patient’s preserved systolic function. Option D, increased sympathetic
activation, can acutely increase contractility but does not account for structural
hypertrophy seen on echocardiography (McCance & Huether, pp. 1125–1126).
4.
A 70-year-old female presents with chest pressure and diaphoresis. ECG reveals
ST-segment elevations in leads II, III, and aVF. Serial cardiac biomarkers are
drawn. Which marker is most specific for myocardial necrosis in this patient?
A. CK-MB
B. Myoglobin
C. Troponin I
D. LDH-1
Correct Answer: C. Troponin I
Rationale:
Troponin I is the most specific and sensitive biomarker for myocardial necrosis. It
, 4
begins to rise within 3–4 hours after myocardial injury, peaks at 10–24 hours, and
remains elevated for 7–10 days, making it ideal for diagnosing both acute and
recent infarctions. CK-MB is relatively specific for cardiac muscle but returns to
baseline within 48–72 hours, making it less useful for late diagnosis. Myoglobin
rises quickly but is nonspecific, as it is present in all muscle tissue. LDH-1 is
outdated as a diagnostic marker due to poor specificity and delayed elevation
(McCance & Huether, p. 1202).
5.
A 76-year-old male with a long history of a heart murmur reports progressive
exertional dyspnea, chest pain, and episodes of dizziness. Physical examination
reveals a late-peaking systolic murmur at the right second intercostal space
radiating to the carotids and diminished carotid upstrokes. Which pathophysiologic
change is occurring in his left ventricle?
A. Eccentric hypertrophy from volume overload
B. Concentric hypertrophy from pressure overload
C. Myocyte atrophy from reduced workload
D. Chamber dilation from reduced compliance
Correct Answer: B. Concentric hypertrophy from pressure overload
Rationale:
Aortic stenosis creates a fixed outflow obstruction that increases left ventricular
afterload. In response, the myocardium undergoes concentric hypertrophy,
characterized by parallel addition of sarcomeres that thicken the ventricular wall
while preserving chamber size. This adaptation helps maintain cardiac output but
eventually reduces ventricular compliance and contributes to diastolic dysfunction.
Option A, eccentric hypertrophy, occurs with chronic volume overload (e.g., mitral
or aortic regurgitation). Option C, myocyte atrophy, is not a feature of aortic
stenosis. Option D, chamber dilation, can occur in the later stages of aortic stenosis
when systolic dysfunction develops, but early disease is defined by hypertrophy
without dilation (McCance & Huether, pp. 1189–1190).
